Obesity results from excessive accumulation of fat in the body. It is caused by ingestion of greater amounts of food than can be used by the body for energy. The excess food, whether fats, carbohydrates, or proteins, is then stored almost entirely as fat in the adipose tissue, to be used later for energy. There can be various causes of obesity including, psychogenic, neurogenic, genetic, and other metabolic related factors. Treatment of obesity depends on decreasing energy input below energy expenditure. Treatment has included among other things, various drugs, starvation and even stapling or surgical resection of a portion of the stomach.
The vagus nerve (which is the 10th cranial nerve) plays a role in mediating afferent information from the stomach to the satiety center in the brain. Afferent neuromodulation of the vagus nerve has also shown to have clinical efficacy for various neurological and neuropsychiatric disorders, such as partial complex epilepsy, generalized epilepsy, Parkinsonson's disease, migraines, depression, Alzheimer's disease, anxiety disorders, obsessive compulsive disorders, and the like. The vagus nerve arises directly from the brain, but unlike other cranial nerves extends well beyond the head. At its farthest extension it reaches the lower parts of the intestines. FIG. 1 shows simplified partial innervation of the vagus nerve and FIG. 2 depicts visceral innervation of the vagus nerve in more detail. Since vagus nerve(s) 54 extend to the sub-diaphragmatic region, they can be selectively stimulated from the anywhere along their length, as described later.
Observations on the profound effects of electrical stimulation of the vagus nerve on central nervous system (CNS) activity extends back to the 1930's. In 1988 it was reported in the American Journal of Physiology, that the afferent vagal fibers from the stomach wall increased their firing rate when the stomach was filled. One way to look at this regulatory process is to imagine that the drive to eat, which may vary rather slowly with the rise and fall of hormone Leptin, is inhibited by satiety signals that occur when we eat and begin the digestive process (i.e., the prandial period). As shown schematically in the top part of FIG. 3, these satiety signals both terminate the meal and inhibit feeding for some time afterward. During this postabsorptive (fasting) period, the satiety signals slowly dissipate until the drive to eat again takes over
The regulation of feeding behavior is a complex process, and involves the concentrated action of several satiety signals such as gastric distention, the release of the gastrointestinal peptide cholecystokinin (CCK), and the release of the pancreatic hormone insulin. The stomach wall is richly innervated by mechanosensory axons, and most of these ascend to the brain via the vagus nerve 54. The vagus sensory axons activate neurons in the Nucleus of the Solitary Tract in the medulla of the brain (described later in this application). These signals inhibit feeding behavior. In a related mechanism, the peptide CCK is released in response to stimulation of the intestines by certain types of food, especially fatty ones. CCK reduces frequency of eating and size of meals. As shown schematically in FIG. 4, both gastric distension and CCK act synergistically to inhibit feeding behavior.
Accordingly, appropriate extra-physiologic electrical stimulation of a vagus nerve 54 or both vagus nerves, from just above the stomach level, should produce appetite suppression by causing the patient to experience satiety. This is shown schematically in FIG. 5A in the form of subdiaphramatic bilateral stimulation. FIGS. 5B-5E show the same concept in alternative embodiments. For example, in FIG. 5B is shown bilateral subdiaphramatic stimulation using two separate pulse generators. FIG. 5C shows supradiaphramatic bilateral stimulation using two separate implanted stimulators. FIG. 5D shows unilateral stimulation, and FIG. 5E shows gastric stimulation. All of these embodiments are considered within the scope of this disclosure.
In one aspect, upon experiencing the compulsive craving, the obese patient can voluntarily activate the stimulus generator by activating a predetermined program. In another aspect, the patient receives chronic stimulation according to a predetermined program whereby stimulation is on for a period of time, followed by off-time in repeating cycles
Prior art search discloses essentially “cardiac pacemaker-like” technology applied to stimulating a vagus nerve. U.S. Pat. Nos. 5,188,104 and 5,263,480 both granted to Wernicke et al. are generally directed to treatment of eating disorders by nerve stimulation. U.S. Pat. Nos. 4,702,254, 4,867,164, and 5,025,807, granted to Zabara are generally directed to neurological disorders. Such system and method, though convenient has the disadvantage that the internal battery will not last for a desired period of time, which can lead to repeated surgeries for pulse generator replacement. Also, because of the concern for reasonable battery longevity, optimal therapy of giving electrical pulses is usually not utilized, since that would lead to excessive drain on the battery. Further, the programming of the stimulation parameters is performed by the medical staff and requires a visit to the physician's office or the clinic, when a program change has to be made. Thus, the prior art has a cumbersome process of adjusting the therapy levels, in addition to the short battery life.
An inductively coupled system and method for neuromodulation granted to Boveja (one of the inventors of the instant application) U.S. Pat. Nos. 6,205,359 B1, 6,269,270 B1, and 6,356,788 B2 overcomes many of the disadvantages of an IPG system such as battery life, and easier activation of programs by the patient, but patient convenience remains an issue since a secondary coil has to be kept in close proximity to an implanted primary coil. It would be ideal to have the advantages of both an IPG system and an inductively coupled system. The system and method disclosed, provides an improved method and system for adjunct therapy by providing a system that has the benefits of both systems, and has additional synergistic benefits not possible in the prior art.
The current application discloses an implantable medical device capable of being used as a programmable implanted pulse generator (IPG), or as a stimulus-receiver for an inductively coupled system with power being supplied by an external stimulator 42, as is shown in FIG. 6. In the bottom right part of FIG. 6, is depicted the programming of the implanted stimulator 75 via a programmer 85. Once programmed, the implanted stimulator 75 functions on its own, as shown on the top part of the figure. As shown in the lower left part of FIG. 6, in the other mode of operation the implanted system 75 can be used as a stimulus-receiver where the power is being supplied from an external stimulator unit 42. In this system and method, the patient can choose when to use an external inductively coupled system to conserve the battery life of the implanted module and receive higher levels of therapy, or be stimulated by the internal system for convenience.
FIG. 7 shows a close up view of the implanted stimulator 75, showing the two subassemblies 68, 70. The two subassemblies are the stimulus-receiver module 68 and the battery operated pulse generator module 70. The external stimulator 42, and programmer 85 also being remotely controllable from a distant location via the internet. Controlling circuitry means within the device, makes the inductively coupled stimulator and the IPG operate in harmony with each other, as described later. For example, when stimulation is applied via the inductively coupled system, the battery operated portion of the stimulator is triggered to go into the “sleep” mode. Conversely, when programming pulses (which are also inductively coupled) are being applied to the implanted battery operated pulse generator, the inductively coupled stimulation circuitry is disconnected.
In the system and method of the current invention, after the system is implanted in the patient, optimal stimulation parameters are “titrated” for the condition of the individual patent. Clinical research has shown that each patient is biologically unique and responds little bit differently to given stimulation. The inductively coupled stimulation part of the system is a very convenient method of adjusting the parameters for stimulation therapy, that would be optimally suited for each individual patient. Further, as depicted in FIG. 8, the external stimulator 42 has a telemetry module and can be controlled remotely via the internet. In one embodiment, numerous pre-determined programs are pre-packaged into the memory of the external stimulator 42. A physician or medical personnel situated remotely is able to selectively activate (and de-activate) selected pre-packaged (pre-determined) programs. As shown in FIGS. 9A and 9B, the telemetry module within the external stimulator wirelessly communicates with a base station 2, either via an attachment as shown in FIG. 9A, or directly as shown in FIG. 9B. Also, as shown in FIG. 10, a physician in a remote location is able to interrogate and selectively program the external stimulator 42 via a server 130.
Once the appropriate stimulation parameters are determined by “trial and error”, the battery operated portion of the implanted pulse generator 70 can be programmed to the optimal electrical stimulation parameters via a programmer 85. For ideal therapy, the electrical stimulation parameters need to be adjusted at regular intervals taking into account optimal benefits.
Another distinct advantage of the current system is that when the stimulation is performed via the external stimulator 42, the battery of the implanted pulse generator (IPG) 70 is conserved, extending the life of the implanted system 75.